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[Cancer Research 59, 947-952, February 1, 1999]
© 1999 American Association for Cancer Research

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[Cancer Research 59, 947-952, February 15, 1999]
© 1999 American Association for Cancer Research


Tumor Biology

Cadherin-11 Is Expressed in Invasive Breast Cancer Cell Lines1

Michael J. Pishvaian, Carolyn M. Feltes, Patrick Thompson, Marion J. Bussemakers, Jack A. Schalken and Stephen W. Byers2

The Lombardi Cancer Research Center and the Department of Cell Biology, Georgetown University School of Medicine, Washington, DC 20007 [M. J. P., C. M. F., P. T., S. W. B.], and Urology Research Laboratory, University Hospital Nijmegen, the Netherlands [M. J. B., J. A. S.]

In several cancers, including breast cancer, loss of E-cadherin expression is correlated with a loss of the epithelial phenotype and with a gain of invasiveness. Cells that have lost E-cadherin expression are either poorly invasive with a rounded phenotype, or highly invasive, with a mesenchymal phenotype. Most cells lacking E-cadherin still retain weak calcium-dependent adhesion, indicating the presence of another cadherin family member. We have now examined the expression of the mesenchymal cadherin, cadherin-11, in breast cancer cell lines. Cadherin-11 mRNA and protein, as well as a variant form, are expressed in the most invasive cell lines but not in any of the noninvasive cell lines. Cadherin-11 is localized to a detergent-soluble pool and is associated with both {alpha}- and ß-catenin. Immunocytochemistry shows that cadherin-11 is localized to the cell membrane at sites of cell-cell contact as well as at lamellipodia-like projections, which do not interact with other cells. These results suggest that cadherin-11 expression may be well correlated with the invasive phenotype in cancer cells and may serve as a molecular marker for the more aggressive, invasive subset of tumors. Cadherin-11 may mediate the interaction between malignant tumor cells and other cell types that normally express cadherin-11, such as stromal cells or osteoblasts or perhaps even with the surrounding extracellular matrix, thus facilitating tumor cell invasion and metastasis.




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Copyright © 1999 by the American Association for Cancer Research.